Hyperoside inhibits lipopolysaccharide-induced mastitis in mice by inactivating the NLRP3 inflammasome

Abstract

IntroductionThe impact of bovine mastitis on animal husbandry is great huge. It is anincurable an incurable disease mainly characterized by milk and pathological changes in milk and the mammary gland, which causescause reduced yield and quality of milk, but. Unfortunately, the use of antibiotics to combat mastitis affects the production of milk, so it is urgent to find additional therapeutic molecules for mastitis treatment.Material and methodsIn this study, we analyzed the protection provided by hyperoside (HYP) in a model of mastitis in vivo and explored its functional mechanism in mouse mammary epithelial cells (mMECs) by overexpression of NOD-, LRR- and pyrin domain-containing 3 (NLRP3).ResultsOur results showed that HYP at 12.5, 25 and 50 mg/kg prevented the inflammatory response induced in lipopolysaccharide (LPS)-stimulated micemouse mammary glands as well as inflammatory cytokine production, including tumor necrosis factor (TNF)-α, interleukin (IL)-6, IL-1β and IL-8. The protection provided by HYP was also correlated with the reduction of NLRP3 signaling pathway protein levels in vivo. However, overexpression of NLRP3 reversed the effects of HYP on the NLRP3 inflammasome, cell viability and inflammatory factor levels in LPS-stimulated mMECs.ConclusionsIn summary, this study showed that HYP inhibited LPS-stimulated symptoms of breast inflammation by regulating expression of inflammatory cytokines and inhibiting the NLRP3 signaling pathway.